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December 2 2015. The December 2015 issue of The FASEB Journal reports the discovery of researchers in China of an ability of ionic magnesium (Mg2+) to help reduce the deposition of amyloid beta in a mouse model of Alzheimer’s disease.

For their research, Pu Wang, PhD, of Northeastern University in Shenyang, China and colleagues tested the effect of magnesium threonate, which is believed to penetrate the blood brain barrier, on normal mice and mice that overexpressed a gene that increased amyloid beta production while decreasing the influx of magnesium into the brain. Among those that received magnesium, the researchers observed a reduction in amyloid beta aggregation and associated cognitive decline, accompanied by an elevation in brain levels of ionic magnesium.

“We hope that our findings will help improve clinical practice pertinent to the optimal administration of Mg2+ for delaying or even preventing the onset of AD,” commented Dr Wang, of Northeastern University’s College of Life and Health Sciences. “Moreover, we hope to extend our experimental models to other disorders such as severe craniocerebral injury, bronchial asthma, chronic pulmonary heart disease, arrhythmia and myocardial necrosis, etc. and identify more targets of Mg2+ and strategies for treating these disorders.”

“The good news about this work is that if it holds up in humans, magnesium is a common element that is readily available,” commented Gerald Weissmann, MD, who is Editor-in-Chief of The FASEB Journal. “The bad news, of course, is that what works in mice does not always turn out so well in people. At the same time, even if magnesium ions do not work out for people with Alzheimer’s, this report will help researchers learn how to slow the development amyloid plaques, a hallmark of the disease.”